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Current Selection
Scheme : NHMRC Project Grants
Research Topic : CELL TRANSFORMATION
Status : Closed
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  • Funded Activity

    Use Of Genetically Altered Immature Bone Marrow Cells T O Induce Leukaemia

    Funder
    National Health and Medical Research Council
    Funding Amount
    $398,969.00
    More information
    Funded Activity

    Chatacterization Of The 43 KDa Inositol Polyphosphate 5-phosphatase

    Funder
    National Health and Medical Research Council
    Funding Amount
    $329,722.00
    More information
    Funded Activity

    A System To Study Cancer Development By Causing Genetic Changes In Blood Cells

    Funder
    National Health and Medical Research Council
    Funding Amount
    $209,269.00
    More information
    Funded Activity

    Identification Of Epstein-Barr Virus Transformation Gen Es.

    Funder
    National Health and Medical Research Council
    Funding Amount
    $91,726.00
    More information
    Funded Activity

    MOLECULAR CELL BIOLOGICAL ANALYSIS OF CAVEOLIN SECRETION

    Funder
    National Health and Medical Research Council
    Funding Amount
    $536,657.00
    Summary
    Aggressive forms of prostate cancer are associated with the release of a protein, called caveolin, from the cancerous cells. Caveolin is normally embedded in the cell surface and drives the formation of microscopic pits termed caveolae. In this proposal we will investigate how caveolin is secreted with a long-term goal of preventing the secretion, or the action, of caveolin.
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    Funded Activity

    Molecular Regulation Of Tumourigenesis By The Polarity Determinant Scribble And Associated Proteins

    Funder
    National Health and Medical Research Council
    Funding Amount
    $614,421.00
    Summary
    Cell polarity is the property of cells to be spatially oriented in a tissue or organ. We have shown that Scribble, a key regulator of cell orientation, may keep tumour development in check. In this proposal, we will examine how disruption of Scribble promotes breast cancer using a combination of tissue culture studies and a newly established mouse model. Understanding how this new pathway can regulate breast tumour development may provide novel targets for therapeutic intervention in cancer.
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    Funded Activity

    Genetic Changes In A Model Of Virally-induced Human Can Cer

    Funder
    National Health and Medical Research Council
    Funding Amount
    $190,284.00
    More information
    Funded Activity

    C-Kit Signalling And Cellular Responses In Haemopoietic Cells

    Funder
    National Health and Medical Research Council
    Funding Amount
    $731,115.00
    Summary
    Growth factors acting on cell surface receptors activate multiple intracellular signalling pathways that regulate cellular growth and function. Mutations in the genes that code for these receptors or their downstream signalling pathways contribute to many human cancers. The contributions of different signalling pathways linked to these receptors to the various cellular responses (growth, maturation, functional activation) are not understood. In this project we aim to use cell and molecular biolo .... Growth factors acting on cell surface receptors activate multiple intracellular signalling pathways that regulate cellular growth and function. Mutations in the genes that code for these receptors or their downstream signalling pathways contribute to many human cancers. The contributions of different signalling pathways linked to these receptors to the various cellular responses (growth, maturation, functional activation) are not understood. In this project we aim to use cell and molecular biology approaches to determine the role of different signalling pathways in cellular responses mediated by the growth factor receptor c-Kit. The c-Kit receptor has essential functions in blood cell development, skin and hair pigmentation, gut function and the reproductive system. It is also essential for the development and function of mast cells which trigger allergic responses such as asthma and eczema. Mutant forms of the receptor have been identified in certain leukaemias and colon cancers. Many new drugs that target specific intracellular signalling pathways have recently been developed and are beginning to be evaluated in clinical trials. Better understanding of how individual pathways contribute to the function of c-Kit and other receptors is essential for optimal use of these new drugs. For example, it may enable the choice of drugs to block c-Kit dependent cancer cell growth or allergic reactions without affecting the growth of normal blood cells.
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    Funded Activity

    Target Genes And Effects On Cell Survival Of The Myb Oncoprotein In Myeloid Cells

    Funder
    National Health and Medical Research Council
    Funding Amount
    $166,408.00
    More information
    Funded Activity

    The Role Of A Phosphorylated Ser/Tyr Bidentate Motif In Leukemia And Myeloproliferative Disorders

    Funder
    National Health and Medical Research Council
    Funding Amount
    $279,254.00
    Summary
    The ability of a normal cell to survive and grow is subject to tight control. Cancer cells escape both these controls and survive and grow in an deregulated manner. Many therapies that are in clinical use or in pre-clinical development target the growth of cancer cells. While such an approach has the advantage of being highly effective in stopping the advance of cancer cell growth, it may allow the long-term survival of some cancer cells and increase the possibility that these cells will become .... The ability of a normal cell to survive and grow is subject to tight control. Cancer cells escape both these controls and survive and grow in an deregulated manner. Many therapies that are in clinical use or in pre-clinical development target the growth of cancer cells. While such an approach has the advantage of being highly effective in stopping the advance of cancer cell growth, it may allow the long-term survival of some cancer cells and increase the possibility that these cells will become resistant to drug treatment leading to disease relapse. On the other hand, therapies that target the survival of malignant cells would be expected to pull the rug from underneath cancer by killing the malignant cells regardless of whether they are growing or not. We have identified a signalling device in normal blood cells that controls both the growth and survival of cells. This device is in effect a switch with 2 components both of which are normally turned on and off. These 2 components are differentially wired to to the cell transmitting unique signals. Importantly, we have found that this switch is faulty in blood cancers and is permanently on in some leukemias promoting their prolonged life-span. Targetting specific components of this unregulated switch may provide new and improved approaches for the development of therapeutics in the treatment of leukemia.
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